Article citations

    R. Zakharyan and A. Boyajyan, “Inflammatory cytokine network in schizophrenia,” World Journal of Biological Psychiatry, 2013.

has been cited by the following article:

  • TITLE: Cryoglobulins as Potential Triggers of Inflammation in Schizophrenia
  • AUTHORS: Andranik Chavushyan,Meri Hovsepyan,Anna Boyajyan
  • JOURNAL NAME: Schizophrenia Research and Treatment DOI: 10.1155/2013/125264 Sep 17, 2014
  • ABSTRACT: This case study aimed to investigate effects of type III cryoglobulins isolated from the blood of patients with schizophrenia on the production of proinflammatory cytokines interleukin(IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α), anti-inflammatory cytokine IL-10, and chemotactic cytokines IL-8 and monocyte chemoattractant protein-1 (MCP-1) by peripheral blood mononuclear cells (PBMCs). The experiments were performed in vitro using PBMCs healthy subjects and the blood of patients whit schizoprenia. The enzyme-linked immunosorbent assay and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay were used upon study. The results obtained indicated significant increase ( ) in IL-1β, IL-6, TNF-α, IL-8, and MCP-1 production by cultured PBMCs when incubating for 24 hours with cryoglobulins, beginning from 0.4?mg/mL. The gender difference does not affect the cryoglobulins-induced production of these cytokines by PBMCs. No influence of cryoglobulins on production of IL-10 by PBMCs was observed. Also, it was shown that cryoglobulins in concentration ≤4?mg/mL possessed no cytotoxic effect towards cultured PBMCs. Based upon the results obtained, we concluded that type III cryoglobulins are implicated in schizophrenia-associated alterations in the immune response through induction of the expression of proinflammatory and chemotactic cytokines by PBMCs. 1. Introduction A considerable evidence suggests a role for upregulated immune response in the pathogenesis of schizophrenia (SCZ), since alterations in both the innate and adaptive immunity including autoimmune and inflammatory components were described in this pathology at both central and peripheral levels [1–7]. Moreover, according to a genetic-vascular-inflammatory hypothesis based upon a number of epidemiologic, clinical, and experimental studies, SCZ generates from a damage of the brain microvascular system initiated by genetically induced upregulated inflammatory reactions developed in response to ubiquitous environmental factors [8]. The results of our previous study revealed the detectable blood levels of type III cryoglobulins (Cgs) in SCZ and found the presence of complement activation split products in these complexes [9]. The presence of Cgs in the blood is detected in lymphoproliferative, autoimmune and infectious diseases and considered as a marker of the immune system chronic activation, inflammation, and autoimmune sensitization [10, 11]. Cgs can cause immune complex vacuities by depositing in the blood vessels, bind complement components, activate the complement system, and induce